Challenges in the diagnosis and management of sleeping sickness in Tanzania: a case report.

In Tanzania sleeping sickness presents a serious threat to human health with a country-wide average of 400 cases reported annually. Both wild and domestic animals have been found to play a significant role in the epidemiology of sleeping sickness. Serengeti National Park in northern Tanzania, has experienced a number of sleeping sickness epidemics since 1922. The epidemics were associated with abundant game animals in the areas and Glossina swynnertoni was incriminated as the main vector. However since 2001 there has been no case of sleeping sickness reported from the park. This case report highlights on the possibility of resurgence and challenges in the diagnosis and management of sleeping sickness in Serengeti. A 38 years old Tanzanian man working in the Serengeti National Park who had experienced various tsetse bites was presented with a febrile condition and history of unsuccessful case management at different health facilities. Blood and cerebrospinal fluid (CSF) samples were examined for the presence oftrypanosomes using wet film, Field's stain and concentration techniques. Typanosoma brucei rhodesiense were detected in both the blood and CSF samples. The patient was treated successfully with melarsoprol. The results of this case study highlight the possibility of resurgence of sleeping sickness in the park hence calls for the need to create more awareness among the community and clinicians. There is need for early reporting to health facility and strengthening the diagnostic capacity of healthcare facilities in and around national parks endemic for sleeping sickness.

Drug-resistance of Trypanosoma b. rhodesiense isolates from Tanzania.

OBJECTIVE: To determine the drug resistance of Trypanosoma brucei rhodesiense strains isolated from sleeping sickness patients in Tanzania. METHOD: We first screened 35 T. b. rhodesiense strains in the mouse model, for sensitivity to melarsoprol (1.8, 3.6 and 7.2 mg/kg), diminazene aceturate (3.5, 7 and 14 mg/kg), suramin (5, 10 and 20 mg/kg) and isometamidium (0.1, 1.0 and 2 mg/kg). A 13 isolates suspected to be resistant were selected for further testing in vitro and in vivo. From the in vitro testing, IC(50) values were determined by short-term viability assay, and MIC values were calculated by long-term viability assay. For in vivo testing, doses higher than those in the initial screening test were used. RESULTS: Two T. b rhodesiense stocks expressed resistance in vivo to melarsoprol at 5 mg/kg and at 10 mg/kg. These strains had high IC(50) and MIC values consistent with those of the melarsoprol-resistant reference strain. Another isolate relapsed after treatment with 5 mg/kg of melarsoprol although it did not appear resistant in vitro. One isolate was resistant to diminazene at 14 mg/kg and another was resistant at both 14 and 28 mg/kg of diminazene. These two isolates had high IC(50) values consistent with the diminazene-resistant reference strain. Two isolates relapsed at a dose of 5 mg/kg of suramin, although no isolate appeared resistant in the in vitro tests. Two isolates were resistant to isometamidium at 1.0 mg/kg and had higher IC(50) values. Two isolates were cross-resistant to melarsoprol and diminazene and one isolate was cross-resistant to suramin and isometamidium. CONCLUSION: The reduced susceptibility of T. b. rhodesiense isolates to these drugs strongly indicates that drug resistance may be emerging in north-western Tanzania.